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Characterization of Eicosanoids Produced by Adipocyte Lipolysis: IMPLICATION OF CYCLOOXYGENASE-2 IN ADIPOSE INFLAMMATION
Journal article   Open access   Peer reviewed

Characterization of Eicosanoids Produced by Adipocyte Lipolysis: IMPLICATION OF CYCLOOXYGENASE-2 IN ADIPOSE INFLAMMATION

Allison Gartung, Jiawei Zhao, Simon Chen, Emilio Mottillo, Garrett C VanHecke, Young-Hoon Ahn, Krishna Rao Maddipati, Andrey Sorokin, James Granneman and Menq-Jer Lee
The Journal of biological chemistry, v 291(31), pp 16001-16010
29 Jul 2016
DOI: https://doi.org/10.1074/jbc.M116.725937
PMID: 27246851
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
http://www.jbc.org/content/291/31/16001.full.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1074/jbc.M116.725937View
Published, Version of Record (VoR) Open

Abstract

3T3-L1 Cells Adipocytes - enzymology Adipocytes - pathology Animals Chemokine CCL2 - metabolism Cyclooxygenase 2 - biosynthesis Eicosanoids - biosynthesis Inflammation - enzymology Inflammation - pathology Lipolysis Macrophages - metabolism Macrophages - pathology MAP Kinase Kinase 4 - metabolism Mice NF-kappa B - metabolism Panniculitis - enzymology Panniculitis - pathology Signal Transduction Sterol Esterase - metabolism
Excessive adipocyte lipolysis generates lipid mediators and triggers inflammation in adipose tissue. However, the specific roles of lipolysis-generated mediators in adipose inflammation remain to be elucidated. In the present study, cultured 3T3-L1 adipocytes were treated with isoproterenol to activate lipolysis and the fatty acyl lipidome of released lipids was determined by using LC-MS/MS. We observed that β-adrenergic activation elevated levels of approximately fifty lipid species, including metabolites of cyclooxygenases, lipoxygenases, epoxygenases, and other sources. Moreover, we found that β-adrenergic activation induced cyclooxygenase 2 (COX-2), not COX-1, expression in a manner that depended on activation of hormone-sensitive lipase (HSL) in cultured adipocytes and in the epididymal white adipose tissue (EWAT) of C57BL/6 mice. We found that lipolysis activates the JNK/NFκB signaling pathway and inhibition of the JNK/NFκB axis abrogated the lipolysis-stimulated COX-2 expression. In addition, pharmacological inhibition of COX-2 activity diminished levels of COX-2 metabolites during lipolytic activation. Inhibition of COX-2 abrogated the induction of CCL2/MCP-1 expression by β-adrenergic activation and prevented recruitment of macrophage/monocyte to adipose tissue. Collectively, our data indicate that excessive adipocyte lipolysis activates the JNK/NFκB pathway leading to the up-regulation of COX-2 expression and recruitment of inflammatory macrophages.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biochemistry & Molecular Biology
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